Environmental Factors That Disrupt Leydig Cell Steroidogenesis

Papadopoulos, Vassilios

doi:10.1007/978-1-59745-453-7_28

Cited by 5 publications

(3 citation statements)

References 270 publications

(332 reference statements)

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“…A number of xenotoxicants have been shown to have selective reproductive toxicity in the rat (e.g. bisphenol A, phthalates, polyaromatic hydrocarbons, molinate) acting primarily on the Sertoli cells (Boekelheide et al 2005) and Leydig cells (Ellis et al 1998, Papadopoulos 2007 and leading to disruption of spermatogenesis. Xenobiotic metabolism by the Leydig cells may act to limit and reduce the effects of these, and other, compounds as Expression of selected proteins in the adult rat testis.…”

Section: Discussionmentioning

confidence: 99%

Identification of Leydig cell-specific mRNA transcripts in the adult rat testis

O’Shaughnessy¹,

Monteiro²,

Fowler³

et al. 2014

Reproduction

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The adult population of Leydig cells acts to secrete testosterone which is essential for reproductive health and fertility in the adult male. However, other physiological functions of these cells are uncertain, and to address this issue a cell ablation model has been used to identify Leydig cell-specific mRNA transcripts. Ethane dimethane sulphonate (EDS) was synthesised by a novel process and was used to ablate Leydig cells in adult male rats previously treated with butane dimethane sulphonate (busulphan) to delete the germ cell population. Levels of mRNA transcripts were measured in the testis using microarrays 1, 3, 5, 8 and 12 days after EDS injection. During this period, there was a significant change in the levels of 2200 different transcripts with a marked decline in the levels of canonical Leydig cell transcripts, such as Cyp11a1, Cyp17a1 and Insl3. A total of 95 transcripts showed a similar decline in expression after EDS treatment, suggesting that they have a Leydig cell-specific origin. Analysis of selected transcripts confirmed that they were expressed specifically in Leydig cells and showed that most had a late onset of expression during adult Leydig cell development. Apart from transcripts encoding components of the steroidogenic apparatus, the most common predicted function of translated proteins was endogenous and xenotoxicant metabolism. In addition, a number of transcripts encode acute-phase proteins involved in reduction of oxidative stress. Results show that, in addition to androgen secretion, Leydig cells may have a critical role to play in protecting the testis from damage caused by toxicants or stress.

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Section: Discussionmentioning

confidence: 99%

Identification of Leydig cell-specific mRNA transcripts in the adult rat testis

O’Shaughnessy¹,

Monteiro²,

Fowler³

et al. 2014

Reproduction

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“…Leydig cells (LC) of the testes are responsible for the biosynthesis and secretion of androgens, critical for developmental and reproductive function in the male. Disruption of testosterone biosynthesis by environmental factors can cause sexual dysfunction, infertility, or sterility (Papadopoulos 2007).…”

Section: Introductionmentioning

confidence: 99%

Effects of scrotal hyperthermia on Leydig cells in long-term: a histological, immunohistochemical and ultrastructural study in rats

Kanter

Aktaş

2009

J Mol Hist

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We have previously demonstrated that scrotal hyperthermia induce Leydig cell (LC) damage in short-term. The objectives of this pilot study were to investigate morphological changes and regulation of steroidogenesis on LC in long-term and the time of observation were extended to investigate whether the LC would eventually make a recovery after scrotal hyperthermia. The rats were randomly allotted into one of four groups: A (control), B (70 days after scrotal hyperthermia), C (105 days after scrotal hyperthermia), D (140 days after scrotal hyperthermia); each group contain seven animals. Scrotal hyperthermia was carried out in a thermostatically controlled water bath at 43 degrees C for 30 min once daily for six consecutive days. Control rats were treated in the same way, except the testes were immersed in a water bath maintained at 22 degrees C. Hyperthermia applied rats were sacrificed under 50 mg/kg ketamine anaesthesia after 70, 105 and 140 days, and biopsy materials of testes were obtained for light and electron microscopic examinations. Morphologically normal and the number of testosterone positive LC was significantly higher in 140 days after last heat than all other heat treatment groups. In heat treated groups, a dilated smooth endoplasmic reticulum, swollen mitochondria, and vanished mitochondrial cristae were observed. In the 140 days after scrotal hyperthermia, the severities of degenerative changes of LC were less than that observed in the other heat treated groups. We conclude that, scrotal hyperthermia cause morphological damaging and impaired steroidogenesis in LC and recovery of these findings were noted first time in 140 days after the last heat treatment.

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“…The detrimental effects of DEHP administration on the male reproductive tract also have been attributed to MEHP (22). For example, MEHP was shown to inhibit LH-stimulated steroid formation by both purified adult rat Leydig cells and MA-10 mouse tumor Leydig cells (23)(24)(25). The mechanism by which MEHP functions to alter steroidogenesis is uncertain.…”

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confidence: 99%

Molecular Mechanisms Mediating the Effect of Mono-(2-Ethylhexyl) Phthalate on Hormone-Stimulated Steroidogenesis in MA-10 Mouse Tumor Leydig Cells

Fan

Traore

et al. 2010

Endocrinology

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Di-(2-ethylhexyl) phthalate, a widely used plasticizer, and its active metabolite, mono-(2-ethylhexyl) phthalate (MEHP), have been shown to exert adverse effects on the reproductive tract in developing and adult animals. As yet, however, the molecular mechanisms by which they act are uncertain. In the present study, we address the molecular and cellular mechanisms underlying the effects of MEHP on basal and human chorionic gonadotropin (hCG)-stimulated steroid production by MA-10 Leydig cells, using a systems biology approach. MEHP induced dose-dependent decreases in hCG-stimulated steroid formation. Changes in mRNA and protein expression in cells treated with increasing concentrations of MEHP in the presence or absence of hCG were measured by gene microarray and protein high-throughput immunoblotting analyses, respectively. Expression profiling indicated that low concentrations of MEHP induced the expression of a number of genes that also were expressed after hCG stimulation. Cross-comparisons between the hCG and MEHP treatments revealed two genes, Anxa1 and AR1. We suggest that these genes may be involved in a new self-regulatory mechanism of steroidogenesis. The MEHP-induced decreases in hCG-stimulated steroid formation were paralleled by increases in reactive oxygen species generation, with the latter mediated by the Cyp1a1 gene and its network. A model for the mechanism of MEHP action on MA-10 Leydig cell steroidogenesis is proposed.

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Environmental Factors That Disrupt Leydig Cell Steroidogenesis

Cited by 5 publications

References 270 publications

Identification of Leydig cell-specific mRNA transcripts in the adult rat testis

Identification of Leydig cell-specific mRNA transcripts in the adult rat testis

Effects of scrotal hyperthermia on Leydig cells in long-term: a histological, immunohistochemical and ultrastructural study in rats

Molecular Mechanisms Mediating the Effect of Mono-(2-Ethylhexyl) Phthalate on Hormone-Stimulated Steroidogenesis in MA-10 Mouse Tumor Leydig Cells

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